scholarly journals ERG Conductance Expression Modulates the Excitability of Ventral Horn GABAergic Interneurons That Control Rhythmic Oscillations in the Developing Mouse Spinal Cord

2007 ◽  
Vol 27 (4) ◽  
pp. 919-928 ◽  
Author(s):  
F. Furlan ◽  
G. Taccola ◽  
M. Grandolfo ◽  
L. Guasti ◽  
A. Arcangeli ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Ventral Horn ◽  
Gabaergic Interneurons ◽  
Mouse Spinal Cord

scholarly journals Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord

2022 ◽  
Vol 23 (2) ◽  
pp. 834
Author(s):  
Chigusa Shimizu-Okabe ◽  
Shiori Kobayashi ◽  
Jeongtae Kim ◽  
Yoshinori Kosaka ◽  
Masanobu Sunagawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Radial Glia ◽  
Ventricular Zone ◽  
Glycine Receptor ◽  
Ventral Horn ◽  
Gabaergic Neurons ◽  
Inhibitory Neurons ◽  
Gamma Aminobutyric Acid ◽  
Mouse Spinal Cord ◽  
Mature Mouse

Gamma-aminobutyric acid (GABA) and glycine act as inhibitory neurotransmitters. Three types of inhibitory neurons and terminals, GABAergic, GABA/glycine coreleasing, and glycinergic, are orchestrated in the spinal cord neural circuits and play critical roles in regulating pain, locomotive movement, and respiratory rhythms. In this study, we first describe GABAergic and glycinergic transmission and inhibitory networks, consisting of three types of terminals in the mature mouse spinal cord. Second, we describe the developmental formation of GABAergic and glycinergic networks, with a specific focus on the differentiation of neurons, formation of synapses, maturation of removal systems, and changes in their action. GABAergic and glycinergic neurons are derived from the same domains of the ventricular zone. Initially, GABAergic neurons are differentiated, and their axons form synapses. Some of these neurons remain GABAergic in lamina I and II. Many GABAergic neurons convert to a coreleasing state. The coreleasing neurons and terminals remain in the dorsal horn, whereas many ultimately become glycinergic in the ventral horn. During the development of terminals and the transformation from radial glia to astrocytes, GABA and glycine receptor subunit compositions markedly change, removal systems mature, and GABAergic and glycinergic action shifts from excitatory to inhibitory.

scholarly journals Adenosine-mediated modulation of ventral horn interneurons and spinal motoneurons in neonatal mice

2015 ◽  
Vol 114 (4) ◽  
pp. 2305-2315 ◽  
Author(s):  
Emily C. Witts ◽  
Filipe Nascimento ◽  
Gareth B. Miles
Keyword(s):  
Spinal Cord ◽  
Purinergic Signaling ◽  
Presynaptic Receptors ◽  
Ventral Horn ◽  
Cellular Mechanisms ◽  
Mouse Spinal Cord ◽  
Synaptic Inputs ◽  
Adenosine Receptor Antagonist ◽  
Postsynaptic Currents

Neuromodulation allows neural networks to adapt to varying environmental and biomechanical demands. Purinergic signaling is known to be an important modulatory system in many parts of the CNS, including motor control circuitry. We have recently shown that adenosine modulates the output of mammalian spinal locomotor control circuitry (Witts EC, Panetta KM, Miles GB. J Neurophysiol 107: 1925–1934, 2012). Here we investigated the cellular mechanisms underlying this adenosine-mediated modulation. Whole cell patch-clamp recordings were performed on ventral horn interneurons and motoneurons within in vitro mouse spinal cord slice preparations. We found that adenosine hyperpolarized interneurons and reduced the frequency and amplitude of synaptic inputs to interneurons. Both effects were blocked by the A1-type adenosine receptor antagonist DPCPX. Analysis of miniature postsynaptic currents recorded from interneurons revealed that adenosine reduced their frequency but not amplitude, suggesting that adenosine acts on presynaptic receptors to modulate synaptic transmission. In contrast to interneurons, recordings from motoneurons revealed an adenosine-mediated depolarization. The frequency and amplitude of synaptic inputs to motoneurons were again reduced by adenosine, but we saw no effect on miniature postsynaptic currents. Again these effects on motoneurons were blocked by DPCPX. Taken together, these results demonstrate differential effects of adenosine, acting via A1 receptors, in the mouse spinal cord. Adenosine has a general inhibitory action on ventral horn interneurons while potentially maintaining motoneuron excitability. This may allow for adaptation of the locomotor pattern generated by interneuronal networks while helping to ensure the maintenance of overall motor output.

scholarly journals Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord

2021 ◽  
Author(s):  
Chigusa Shimizu-Okabe ◽  
Shiori Kobayashi ◽  
Jeongtae Kim ◽  
Yoshinori Kosaka ◽  
Masanobu Sunagawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Radial Glia ◽  
Ventricular Zone ◽  
Glycine Receptor ◽  
Ventral Horn ◽  
Gabaergic Neurons ◽  
Inhibitory Neurons ◽  
Gamma Aminobutyric Acid ◽  
Mouse Spinal Cord ◽  
Mature Mouse

Gamma-aminobutyric acid (GABA) and glycine act as inhibitory neurotransmitters. Three types of inhibitory neurons and terminals, GABAergic, GABA/glycine co-releasing, and glycinergic, are orchestrated in the spinal cord neural circuits and play key roles in the regulation of pain, locomotive movement, and respiratory rhythms. Herein, we first describe GABAergic and glycinergic transmission and inhibitory networks, which consist of three types of terminals, in the mature mouse spinal cord. Second, we describe the developmental formation of GABAergic and glycinergic networks, with specific focus on the differentiation of neurons, formation of synapses, maturation of removal systems, and changes in their action. GABAergic and glycinergic neurons are derived from the same domains of the ventricular zone. Initially, GABAergic neurons are differentiated and their axons form synapses. Some of these neurons remain GABAergic in lamina I and II. Many of GABAergic neurons convert to co-releasing state. The co-releasing neurons and terminals remain in the dorsal horn, whereas many of co-releasing ones ultimately become glycinergic in the ventral horn. During the development of terminals and the transformation from radial glia to astrocytes, GABA and glycine receptor subunit compositions markedly change, removal systems mature, and GABAergic and glycinergic action shifts from excitatory to inhibitory.

scholarly journals Evidence for glutamine synthetase function in mouse spinal cord oligodendrocytes

2021 ◽  
Author(s):  
Lucile Ben Haim ◽  
Lucas Schirmer ◽  
Amel Zulji ◽  
Khalida Sabeur ◽  
Brice Tiret ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Glutamine Synthetase ◽  
Motor Neurons ◽  
Ventral Horn ◽  
Conditional Knockout ◽  
Oligodendrocyte Progenitor Cells ◽  
Mouse Spinal Cord ◽  
Reporter Mice ◽  
Key Enzyme ◽  
Ventral Spinal Cord

Glutamine synthetase (GS) is a key enzyme that metabolizes glutamate into glutamine. While GS is expressed by astrocytes of the central nervous system (CNS), expression in other glial lineages has been noted. Using a combination of reporter mice and cell type-specific markers, we show that GS is expressed in myelinating oligodendrocytes (OL) but not oligodendrocyte progenitor cells (OPC) of the mouse spinal cord abutting ventral horn motor neurons. To investigate the role of GS in mature OL, we used a conditional knockout (cKO) approach to selectively delete GS-encoding gene (Glul) in OL, which caused a significant decrease in glutamine levels on spinal cord extracts. We evaluated the effect on ventral spinal cord sensorimotor circuits and observed that GS cKO mice (CNP-cre+ : Glul fl/fl) showed no differences in motor neuron numbers, size or axon density; OL differentiation and myelination in the ventral spinal cord at 1- and 6-months of age was normal. Interestingly, GS cKO mice showed an early and specific decrease in peak force while motor function remained otherwise unaffected. These findings provide evidence OL-encoded GS functions in spinal cord sensorimotor circuit.

scholarly journals Characterization of calbindin D28k expressing interneurons in the ventral horn of the mouse spinal cord

2017 ◽  
Vol 247 (1) ◽  
pp. 185-193
Author(s):  
Taylor L. Floyd ◽  
Yiyun Dai ◽  
David R. Ladle
Keyword(s):  
Spinal Cord ◽  
Ventral Horn ◽  
Mouse Spinal Cord ◽  
Calbindin D28k

Antagonist-induced opiate receptor upregulation in cultures of fetal mouse spinal cord-ganglion explants

1986 ◽  
Vol 390 (2) ◽  
pp. 287-291 ◽  
Author(s):  
A TEMPEL ◽  
S CRAIN ◽  
E PETERSON ◽  
E SIMON ◽  
R SUZANNEZUKIN
Keyword(s):  
Spinal Cord ◽  
Opiate Receptor ◽  
Fetal Mouse ◽  
Mouse Spinal Cord ◽  
Receptor Upregulation
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